Effects of Clonality on the Genetic Variability of Rare, Insular Species: The Case of Ruta Microcarpa From the Canary Islands.

Effects of clonality on the genetic variability of rare, insular species: the case of Ruta microcarpa from the Canary Islands.

Ecol Evol. 2013 Jun; 3(6): 1569-1579
Meloni M, Reid A, Caujapé-Castells J, Marrero A, Fernández-Palacios JM, Mesa-Coelo RA, Conti E

Many plant species combine sexual and clonal reproduction. Clonal propagation has ecological costs mainly related to inbreeding depression and pollen discounting; at the same time, species able to reproduce clonally have ecological and evolutionary advantages being able to persist when conditions are not favorable for sexual reproduction. The presence of clonality has profound consequences on the genetic structure of populations, especially when it represents the predominant reproductive strategy in a population. Theoretical studies suggest that high rate of clonal propagation should increase the effective number of alleles and heterozygosity in a population, while an opposite effect is expected on genetic differentiation among populations and on genotypic diversity. In this study, we ask how clonal propagation affects the genetic diversity of rare insular species, which are often characterized by low levels of genetic diversity, hence at risk of extinction. We used eight polymorphic microsatellite markers to study the genetic structure of the critically endangered insular endemic Ruta microcarpa. We found that clonality appears to positively affect the genetic diversity of R. microcarpa by increasing allelic diversity, polymorphism, and heterozygosity. Moreover, clonal propagation seems to be a more successful reproductive strategy in small, isolated population subjected to environmental stress. Our results suggest that clonal propagation may benefit rare species. However, the advantage of clonal growth may be only short-lived for prolonged clonal growth could ultimately lead to monoclonal populations. Some degree of sexual reproduction may be needed in a predominantly clonal species to ensure long-term viability. HubMed – depression


Association of Anxiety With Resistance Vessel Dysfunction in Human Atherosclerosis.

Psychosom Med. 2013 Jun 20;
Stillman AN, Moser DJ, Fiedorowicz J, Robinson HM, Haynes WG

ObjectiveAnxiety predicts cardiovascular events, although the mechanism remains unclear. We hypothesized that anxiety symptoms will correlate with impaired resistance and conduit vessel function in participants aged 55 to 90 years.MethodsAnxiety symptoms were measured with the Symptom Checklist-90-Revised in 89 participants with clinically diagnosed atherosclerotic cardiovascular disease and 54 healthy control participants. Vascular function in conduit arteries was measured using flow-mediated dilatation, and vascular function in forearm resistance vessels (FRVs) was measured using intra-arterial drug administration and plethysmography.ResultsAnxiety symptoms were not associated with flow-mediated dilatation in either group. Participants with atherosclerosis exhibited significant inverse associations of anxiety symptoms with FRV dilatation (acetylcholine: ? = -.302, p = .004). Adjustment for medication, risk factors, and depression symptoms did not alter the association between anxiety and FRV dysfunction, except for body mass index (BMI; anxiety: ? = -.175, p = .060; BMI: ? = -.494, p < .001). Although BMI was more strongly associated with FRV function than anxiety, combined BMI and anxiety accounted for greater variance in FRV function than either separately. Control participants showed no association of anxiety with FRV function.ConclusionsAnxiety is uniquely and substantially related to poorer resistance vessel function (both endothelial and vascular smooth muscle functions) in individuals with atherosclerosis. These relationships are independent of medication, depression, and cardiovascular risk factors, with the exception of BMI. These findings support the concept that anxiety potentially increases vascular events through worsening of vascular function in atherosclerotic disease. HubMed – depression


Serotonin Transporter Gene: Will Epigenetics Prove Less Depressing Than Genetics?

Psychosom Med. 2013 Jun 20;
de Geus EJ, Middeldorp CM

The serotonin transporter gene has been hypothesized to influence, possibly in interaction with environmental factors, the vulnerability for depression. So far, genetic studies have tested the association of the repeat polymorphism (5-HTTLPR) with depression and whether it is moderated by exposure to stressful events. This has not yielded unequivocal results, even across meta-analyses. However, environmental factors may induce epigenetic changes in the structure of DNA that can influence gene expression. These epigenetic effects may be independent of the genetic polymorphisms in the gene region. This editorial reviews an article in this issue that compared the intrapair differences in depressive symptoms in monozygotic twin pairs with the intrapair differences of methylation at cytosine-guanine dinucleotide sites in the promoter region of the serotonin transporter gene. Differences in depressive symptoms were correlated with differences in methylation status, such that higher methylation, which, in this sample of identical twins, must be environmental in origin, is associated with more depressive symptoms. Noteworthy is the fact that the epigenetic effects were independent of the 5-HTTLPR. These results should encourage genome-wide testing of the contribution of epigenetic effects to depression. HubMed – depression


Effectiveness of Group Versus Individual Cognitive-Behavioral Therapy in Patients With Abridged Somatization Disorder: A Randomized Controlled Trial.

Psychosom Med. 2013 Jun 20;
Moreno S, Gili M, Magallón R, Bauzá N, Roca M, Del Hoyo YL, Garcia-Campayo J

ObjectiveTo evaluate the effectiveness and feasibility of a cognitive-behavioral program for patients in primary care units who were diagnosed as having abridged somatization disorder.MethodA multicenter, randomized controlled trial was designed. One hundred sixty-eight patients were recruited from 29 primary care units and randomly assigned to one of three arms: treatment as usual (TAU), individual cognitive-behavioral therapy (CBT), and group CBT. Somatic symptoms were measured using the Screening for Somatoform Disorders and the Severity of Somatic Symptoms scale. The Hamilton Anxiety Rating Scale and the Hamilton Depression Rating Scale were used to assess the severity of anxiety and depression.ResultsIndividual CBT achieves greater changes in the Screening for Somatoform Disorders posttreatment compared with group CBT (mean [95% confidence interval], 14.17 [11.9-16.3] versus 11.63 [9.4-13.7], p < .001). These improvements were observed at 6 and 12 months (p < .001 and p < .001, respectively). For individual CBT versus TAU, the number-needed-to-treat was 8, whereas for group CBT versus TAU, the number-needed-to-treat was 9. Individual CBT treatment resulted in lower anxiety scores compared with group CBT and TAU (7.33 [5.4-9.2] versus 11.47 [9.4-13.9] versus 13.07 [10.9-15.2], p < .001) posttreatment. Individual CBT and group CBT were associated with sustained benefits at 12-month follow-up compared with TAU (8.6 [6.6-10.6] versus 9.28 [7.2-11.2] versus 16.2 [13.9-18.5], p < .001). Depressive symptoms were lower for individual CBT posttreatment than for TAU (6.96 [5.3-8.6] versus 10.87-12.7], p < .01).ConclusionsCBT in individual and group settings results in significant improvements in somatic symptoms among patients with somatoform abridged disorder compared with TAU. Individual CBT results in greater posttreatment improvements at 6-month and 12-month follow-ups.Trial Registrationcurrent controlled trials identifier ISRCTN69944771. HubMed – depression